Parkinson's disease is a neurological disorder that is associated with degeneration of brain dopaminergic systems. It has been suggested that this cell death might be secondary to progressive deleterious effects of dopamine (DA) through the production of reactive oxygen species (ROS). The proto-oncogene, bcl2, has been shown to protect cells against ROS-induced damage in vitro. We thus wanted to know if bcl2 could abrogate the toxic effects of DA on immortalized neural cells. DA caused dose-dependent cell death. The use of confocal microscopy, flow cytometry, and DNA gel electrophoresis indicated that DA caused cell death through an apoptotic process. Moreover, METH caused a marked increase in ROS in these cells. However, overexpression of bcl2 afforded significant protection against DA-induced apoptosis. These results will be discussed in terms of the possibility that dysregulation of the bcl2 protective pathway might play a role in the development of Parkinson's disease.